By Mohammad Fahad Ullah, Aamir Ahmad
This e-book specializes in the prophylactic strength of diet-derived elements in basic prevention of melanoma. it really is written by way of a gaggle of hugely reputed specialists within the sector of nutritional brokers and melanoma chemoprevention. The translational capability of nutritional components from epidemiological, laboratory and scientific stories as prevention method in basic and threat populations is highlighted. The work presents options of routine inclusion of particular nutritional regimens for prevention in addition to healing method for higher administration via adjuvant interventions in melanoma remedy.
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Additional resources for Critical dietary factors in cancer chemoprevention
The elevated copper level in malignant cells facilitates electron transfer between polyphenols and copper leading to formation of Cu(I) whose reoxidation in the presence of molecular oxygen leads to ROS formation (Rahman et al. 1989). This would account for the preferential cytotoxicity of plant polyphenols for cancer cells. In addition to the evidence we have deduced, there is considerable supporting data in the literature which suggests that pro-oxidant action of plant polyphenols rather than their antioxidant property is important for their anticancer properties.
While it is believed that the antioxidant properties of these agents may contribute to lowering the risk of cancer induction by impeding oxidative injury to DNA, it could not account for apoptosis induction and chemotherapeutic observations. We have provided a number of evidence that dietary antioxidants can alternatively switch to a pro-oxidant action in the presence of transition metals such as copper. Such a pro-oxidant action leads to strand breaks in cellular DNA and growth inhibition in cancer cells.
2004) demonstrated that the addition of EGCG and Cu2+ to the growth medium decreased the relative viability of human PCa cells. In a study from our laboratory, EGCG was also found to increase the expression of cell cycle regulatory molecules p21, p16, and p18 while downmodulating the protein levels of cyclin D1, cyclin E, cdk2, cdk4, and cdk6 (Gupta et al. 2003). We then reasoned that the preclinical studies should be carried out in a model system that mimics the PCa development in a similar fashion to human disease.